title: Erythrocyte lysate releases Ca2+ from IP3-sensitive stores and activates Ca(2+)-dependent K+ channels in rat basilar smooth muscle cells.
abstract: Erythrocyte lysate increases intracellular Ca2+ ([Ca2+]i), contracts cerebral arteries and has been suggested to be the causative agent for cerebral vasospasm. However, the mechanism of erythrocyte lysate-induced [Ca2+]i mobilization is not clear. This study was undertaken to investigate the action of erythrocyte lysate on [Ca2+]i mobilization by monitoring [Ca2+]i and the Ca(2+)-dependent K+ channels (KCa) in freshly isolated rat basilar artery smooth muscle cells. In a [Ca2+]i imaging study, erythrocyte lysate produced a biphasic response, a transient peak and a prolonged plateau [Ca2+]i elevation. In the absence of external Ca2+, erythrocyte lysate induced only a transient peak [Ca2+]i response without a marked plateau phase, indicating the [Ca2+]i was Ca2+ released from internal stores. Erythrocyte lysate-induced plateau [Ca2+]i response was resistant to nicardipine, a voltage-dependent Ca2+ channel blocker, but was abolished by EGTA. Elevation of [Ca2+]i induced by erythrocyte lysate contracted smooth muscle cells. In the electrophysiological study, elevation of [Ca2+]i by erythrocyte lysate increased KCa currents in whole-cell patch-clamp configuration. This effect of erythrocyte lysate on KCa was blocked by heparin, an antagonist of IP3 receptors. We conclude that erythrocyte lysate releases Ca2+ from IP3-sensitive intracellular stores and produces Ca2+ entry from voltage-independent Ca2+ pathways.
authors.affiliation: Department of Surgery, University of Chicago, IL, USA.
authors.forename: C J
authors.initials: CJ
authors.lastname: Kim
authors.forename: B K
authors.initials: BK
authors.lastname: Weir
authors.forename: R L
authors.initials: RL
authors.lastname: Macdonald
authors.forename: H
authors.initials: H
authors.lastname: Zhang
mesh_terms: D000818:Animals; D001488:Basilar Artery / Q000166:cytology / Q000502:physiology*; D002118:Calcium / Q000378:metabolism*; D002121:Calcium Channel Blockers / Q000494:pharmacology; D002457:Cell Extracts / Q000494:pharmacology; D002614:Chelating Agents / Q000494:pharmacology; D004285:Dogs; D004533:Egtazic Acid / Q000494:pharmacology; D004912:Erythrocytes / Q000737:chemistry* / Q000378:metabolism; D005260:Female; D007091:Image Processing, Computer-Assisted; D015544:Inositol 1,4,5-Trisphosphate / Q000378:metabolism; D009131:Muscle, Smooth, Vascular / Q000737:chemistry / Q000166:cytology / Q000378:metabolism; D009529:Nicardipine / Q000494:pharmacology; D018408:Patch-Clamp Techniques; D011188:Potassium / Q000378:metabolism; D015221:Potassium Channels / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D014661:Vasoconstriction / Q000187:drug effects / Q000502:physiology*
chemical_list: D002121:Calcium Channel Blockers; D002457:Cell Extracts; D002614:Chelating Agents; D015221:Potassium Channels; D004533:Egtazic Acid; D015544:Inositol 1,4,5-Trisphosphate; D009529:Nicardipine; D011188:Potassium; D002118:Calcium